期刊
BLOOD
卷 117, 期 5, 页码 1565-1573出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2010-06-291633
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资金
- Austrian Science Foundation [FWF-SFB 28]
- Vienna Science and Technology Fund [WWTF-LS07-037]
- GENAU grant (Austromouse II, III)
- Biomodels Austria
- Austrian Science Fund (FWF) [F 2808] Funding Source: researchfish
We generated a transgenic mouse line that expresses the Cre recombinase under the control of the Ncr1 (p46) promoter. Cre-mediated recombination was tightly restricted to natural killer (NK) cells, as revealed by crossing Ncr1-iCreTg mice to the eGFP-LSLTg reporter strain. Ncr1-iCreTg mice were further used to study NK cell-specific functions of Stat5 (signal transducers and activators of transcription 5) by generating Stat5(f/f) Ncr1-iCreTg animals. Stat5(f/f) Ncr1-iCreTg mice were largely devoid of NK cells in peripheral lymphoid organs. In the bone marrow, NK-cell maturation was abrogated at the NK cell-precursor stage. Moreover, we found that in vitro deletion of Stat5 in interleukin 2-expanded NK cells was incompatible with NK-cell viability. In vivo assays confirmed the complete abrogation of NK cell-mediated tumor control against B16F10-melanoma cells. In contrast, T cell-mediated tumor surveillance against MC38-adenocarcinoma cells was undisturbed. In summary, the results of our study show that STAT5 has a cell-intrinsic role in NK-cell development and that Ncr1-iCreTg mice are a powerful novel tool with which to study NK-cell development, biology, and function. (Blood. 2011; 117(5):1565-1573)
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